HTN Flashcards
What is the trend in systolic and diastolic BP over time?
Systolic: increases
Diastolic: increases, plateaus at 55, then decreases
What are the epidemiological differences in HTN among men and women?
Men: higher prevalence until age 55
Women: after age 64, higher prevalence.
Classification of BP?
Normal: 160/>100 (either/or)
Blood pressure= ???
BP= CO*SVR
SVR=systemic vascular resistance
Mean Arterial Pressure= ???
MAP= DBP+ 1/3 (SBP-DBP)
SVR= ???
SVR= MAP-CVP/CO
Risk Factors for HTN:
Age, tobacco, lower SES, obesity, sedentary lifestyle, psychosocial stressors, dietary factors (Na+ intake), family hx.
What is renin?
hormone released from JG cells in kidney in response to hypoperfusion or activation of SNS. Converts ATogen to AT1.
Influence of AT1 receptors on kidney
intrarenal BP constriction to decr GFR, tubules increase Na+, H2O reabs.
AT1 receptor influence on adrenal gland
cortex incr aldosterone secr, medulla incr catecholamine secr
AT1 receptor influence on vascular smooth musc
growth promoting factors lead to atherogenesis, vasconstriction leads to incr arteriolar resistance.
AT1 receptor influence on CNS
incr adrenal drive incr arteriolar resistance and CO, incr ADH to incr H2O abs, and incr thirst to incr H2O intake.
AT1 receptor influence on myocardium
incr contractibility and hypertrophy, decr collagenase activity.
How do you take an accurate BP measurement?
bare arm, not over clothes, cuff covers 2/3 length of arm, lower edge approx 2.5 cm from antecubital fossa, pt and observer don’t talk.
What is pseudoHTN?
Cuff doesn’t fit correctly (usually too small) that squeezes too much and appears like pt has HTN. Cuff too big–> BP appears lower.
What does a difference in BP b/w the two arms of >15 mmHG indicate?
Subclavian stenosis (lower pressure side)
What is the home pressure measurement to be considered HTN?
> 135/>85
What is the initial evaluation of a pt w/ HTN?
ID possible secondary causes, ID other CVD risk factors, assess for target organ damage.
What is masked HTN?
Normotensive in clinic, HTN outside of clinic.
What is nocturnal HTN?
normotensive in the day, peaks at night, can wake pt w/ chest pain
When do you begin medication regiment for HTN?
Stage 2: mix of medication and behavior change
Stage 1: Varies
Pre-HTN: mostly behavior/diet changes
Classes of anti-HTN drugs
ACE inhibitors, AT receptor blickers, Ca++ channel blockers, Diuretics (AACD), beta-blockers, alpha-blockers, direct vasodilators, aldosterone antagonists, direct renin inhibitors, central alpha-agonists.
2014 HTN tx goal:
FDA Black Box warning for pregnant women
ACE-inhibitors, AT receptor blockers, or renin inhibitors should not be used because of potential for damage for developing fetal kidney.
Mechanism of action of ACE inhibitors
binds ACE to incr levels of AT1 and decr levels of AT2. Renin incr. Since AT2 stimulates adrenals, ACE inhibition decr aldosterone levels. Also increase bradykinin levels to produce NO to produce vasodilation. This decr peripheral arterial resistance and intravascular vol.
Side effects of ACE inhibitors
Incr bradykinin in lungs, sensitizes bronchial epithelium to irritants–> dry cough that is dose-dep and req cessation of therapy, change to AT1 receptor blocker.
Incr creatinine, worsening renal funct (incr risk w/ chronic kidney disease, renal artery stenosis, cardiomyopathy, diabetes mellitus)
Sulfhydrul-related effects (captopril)= neutropenia, rash
Hyperkalemia
Angioedema (potentiation of bradykinin)
Mechanism of action of AT receptor-blockers
block pathways independent of RAAS system by selectively blocking AT1 receptor. No effect on bradykinin, lower incidence of kinin-mediated side-effects (cough, angioedema).
Mechanism of action of direct renin inhibitor
Blocks “rate-limiting step” of RAAS. Don’t use in conjunction w/ ACE-1 or ARB (incr CV risks!), w/ similar side effects to ACE inhibitors and ARBs.
Mechanism of action of diuretics
incr urinary excretion of Na+ at various sites in kidney, venodilation, decr intravascular vol, lowering BP.
Subclasses of diuretics
thiazides, loop, potassium-sparing, others.
Side effects of diuretics
volume depletion, hypotension, orthostasis, electrolyte changes, hyperkalemia, ototoxicity, metabolic side effects (hyperglycemia, hypercholesterolemia, hyperuricemia), ED, sulfa-allergy
Aldosterone antagonists mechanism of action and side effects.
antagonist for aldosterone at mineralocorticoid receptors, beneficial in resistant NTH and combined w/ other diuretics. Incr risk of hyperkalemia w/ ACE-I or ARBs. Spironolactone (non-selective) w/ ED or gynecomastia in men and menstrual abnormalities in women. Eplerenone is selective.
Mechanism of action of Calcium-channel blockers (CCB)
L-type calcium channels allow Ca++ influx and smooth much contractions, so when CCBs bind to receptors, vasodilate arteriolar smooth muscle, decr PVR. Dihydropyridine (arteriolar dilation)/non-dihydropyridine (decr Ca+ influx into myocardium)
Side effects of CCBs
Non-dihydropyridines: bradycardia, AV block, constipation
Dihydropyridine: edema, headache, flushing, dizziness, palpitations.
All: gingival hyperplasia, aggravate gastroesophageal reflux due to inhibiton of lower esophageal sphincter contraction.
Outcomes of beta-blockers
Decr CO, inhibit renin secr, inhibit NE release. Reduce HR due to decr automaticity in sinus node (negative chronotropic effect). Reduces ventricular hypertrophy, stroke, heart failure, coronary events, and mortality.
Types of beta-blockers
B1 (selective): myocardium, less airway effects
B2 (non-selective): myocardium, vascular, bronchial cells
Lipid-sol beta-blockers: metabolized by the liver, have shorter half-lives
hydrophilic beta-blockers: kidney, longer half-life
Mechanism of action of beta-blockers
intrinsic sympathomimetic activity (weak beta-adrenergic activation), vasodilatory properties (ex: carvedilol) antagonize alpha-adrenergic receptor and incr NO release, usually not first line agent for HTN tx!
Beta-blocker side effects
bradycardia, heart block, dizziness, bronchospasm, cold extremities (beta2 effect), ED, hyperglycemia, lipid abnormalities (TG elevation, HDL reduction)
CNS effects: fatigue, depression, mental slowness, vivid dreams, dry mouth
Hydralazine mechanism of action
A direct vasodilator that directly relaxes smooth musc, decr PVR, and is usually given w/ a diuretic and beta-blocker to prevent pseudotolerance (tachycardia and volume retention). Metabolism genetically determined (N-acetyltransferase w/ fast or slow acetylators)
Minoxidil mechanism of action
Opens K+ channels in vascular smooth musc w/ similary hemodynamics to hydralazine. Useful in severe HTN. Given w/ a diuretic and beta-blockers to prevent pseudotolerance.
Side effects of Minoxidil
pericardial effusion, tachycardia, facial hirsutism
Mechanism of action of alpha-adrenergic receptor blockers
selective alpha-antagonists that blocks site for NE, decr arteriolar resistance, beneficial to patients w/ prostate symptoms (ex: doxazosin)
Side effects of alpha-adrenergic receptor blockers
postural HTN, dizziness, syncope, reflex tachycardia, nasal congestion, volume expansion
Mechanism of action of central sympatholytics
alpha2 agonists (clonidine, methyldopa) that reduce sympathetic outflow to the heart and bv’s.
Side effects of central sympatholytics
sedation, dry mouth, ED
Clonidine: severe rebound HTN, skin hypersens (patch)
Methyldopa: Coomb’s positive hemolytic anemia, elevated lever function tests.
What combination of HTN drugs should never be prescribed together?
ACE-I and ARBs.
